Brain Research最新文献

{"title":"Pentoxifylline protects memory performance in streptozotocin-induced diabetic rats","authors":"Maram Muhsen ,&nbsp;Karem H. Alzoubi ,&nbsp;Omar F. Khabour ,&nbsp;Nizar Mhaidat ,&nbsp;Abeer Rababa’h ,&nbsp;Shirin Ali ,&nbsp;Anan Jarab ,&nbsp;Samina Salim","doi":"10.1016/j.brainres.2024.149319","DOIUrl":"10.1016/j.brainres.2024.149319","url":null,"abstract":"<div><div>Diabetes, characterized by elevated blood glucose levels and associated organ damage, is reportedly correlated with a<!--> <!-->decline in cognitive functions with a potential involvement of oxidative stress mechanisms. Mitochondria-induced oxidative stress reported to cause hyperglycemia is believed to impair hippocampal neural plasticity, affecting long-term potentiation, and is<!--> <!-->considered crucial for maintaining memory functions. In this study, the neuroprotective effect of Pentoxifylline (PTX) for four weeks, an agent known for antioxidant and anti-inflammatory properties, was examined in an animal model of diabetes. In a streptozotocin (STZ) diabetic model, rats received intraperitoneal PTX (100 mg/kg), and learning and memory functions were tested using the radial arm water maze. STZ-treated diabetic rats exhibited impaired learning and memory functions (short/long-term, P &lt; 0.05), whereas PTX treatment prevented these deficits. PTX treatment normalized diabetes-induced reduction in the protein expression levels of two enzymes of antioxidant defense superoxide dismutase and glutathione peroxidase (P &lt; 0.05) in the hippocampal brain tissues. PTX treatment also mitigated STZ-induced increase in lipid peroxidation (TBARS, P &lt; 0.05). Furthermore, reduced/oxidized glutathione (GSH/GSSG) ratios were enhanced in PTX-treated diabetic rats (P &lt; 0.05), emphasizing the importance of redox balance restoration. However, PTX treatment did not significantly affect the<!--> <!-->antioxidant defense enzyme catalase activity. In conclusion, STZ-induced diabetes resulted in learning and memory impairment in rats, while PTX treatment prevented these effects, most likely via enhancement of antioxidant defense in the brain. This study highlights PTX’s potential neuroprotective benefits, providing translational insights into the issue of diabetes-related cognitive complications.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1847 ","pages":"Article 149319"},"PeriodicalIF":2.7,"publicationDate":"2024-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperfunction of AMPA receptors in the amygdala and hippocampus contributes to enhanced fear memory in diabetic mice","authors":"Megumi Ikegami,&nbsp;Hiroko Ikeda","doi":"10.1016/j.brainres.2024.149327","DOIUrl":"10.1016/j.brainres.2024.149327","url":null,"abstract":"<div><div>Patients with diabetes mellitus show an elevated prevalence of psychiatric disorders such as anxiety. We have reported that fear memory, a model related to anxiety as reflected in the freezing response, is enhanced in diabetic mice and was ameliorated by an AMPA receptor antagonist. The present study investigated whether functions of AMPA receptors in the amygdala and hippocampus are altered in streptozotocin (STZ)-induced diabetic mice. While protein levels of the GluA1 subunit of AMPA receptors were not altered in the amygdala and hippocampus, protein levels of GluA1 phosphorylated at serine 845 in the amygdala and hippocampus and of GluA1 phosphorylated at serine 831 in the hippocampus were increased in STZ-induced diabetic mice. L-lactate, which is increased in the amygdala and hippocampus of STZ-induced diabetic mice, did not alter these protein levels in either brain area. In contrast, protein levels of phosphorylated protein kinase A (PKA) catalytic subunit and phosphorylated calcium calmodulin kinase II (CaMKII), which are known to phosphorylate serine 845 and serine 831 of GluA1, respectively, were increased in the amygdala and hippocampus of STZ-induced diabetic mice. In the fear memory test, the PKA inhibitor H-89 injected before test sessions and the CaMKII inhibitor KN-62 injected before conditioning or test sessions each reduced the increase in freezing in STZ-induced diabetic mice. These results indicate that the functions of AMPA receptors in the amygdala and hippocampus are enhanced due to increased phosphorylation by PKA and CaMKII, which enhances fear memory in diabetic mice.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149327"},"PeriodicalIF":2.7,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chaperone-mediated autophagy (CMA) confers neuroprotection of HBO preconditioning against stroke.","authors":"Lin Yang, Yuan Huang, Yuliang Peng, Qingyu Sun, Ding Zhang, Shulin Yang, Jian Song, Xiaoxiao Sun, Chuan Lv, Xijing Zhang, Zongping Fang","doi":"10.1016/j.brainres.2024.149315","DOIUrl":"https://doi.org/10.1016/j.brainres.2024.149315","url":null,"abstract":"<p><p>Previous attempts to identify neuroprotective targets for acute ischemic stroke by studying ischemic cascades and devising ways to suppress these pathways have failed in translational research. We hypothesized that studying the molecular determinants of endogenous neuroprotection, namely, the tolerance against ischemic stroke conferred by hyperbaric oxygen (HBO) preconditioning, via a well-established paradigm would reveal new neuroprotective targets. By a combination of proteomics, KEGG pathway analysis, lysosome fraction and western blot analysis, we found that chaperone-mediated autophagy (CMA) was activated by HBO preconditioning. In addition, LAMP2A is uniquely decreased in cortical neurons in the early stage of stroke. Suppression of CMA with recombinant adeno-associated viral vector (rAAV)-mediated delivery of short hairpin RNAs (shRNAs) targeting the LAMP2A transcript increased the neuronal susceptibility of apoptosis and abolished the neuroprotection induced by HBO preconditioning. Administration of the clinically utilized FDA-approved drug mycophenolate mofetil induced long-term neuroprotection post-stroke in a CMA-dependent manner. In summary, HBO preconditioning confers neuroprotection against ischemia by inducing CMA, which is a promising translational treatment target for stroke.</p>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":" ","pages":"149315"},"PeriodicalIF":2.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614670","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of NMDA glutamatergic receptors pharmacological stimulation of the ventral tegmental area on the memory deficits induced by maternal deprivation","authors":"Ben-Hur Souto das Neves,&nbsp;Karine Ramires Lima,&nbsp;Ana Carolina de Souza da Rosa,&nbsp;Guilherme Liao,&nbsp;Anna Cecília Perretto,&nbsp;Guilherme Salgado Carrazoni,&nbsp;Pâmela Billig Mello-Carpes","doi":"10.1016/j.brainres.2024.149316","DOIUrl":"10.1016/j.brainres.2024.149316","url":null,"abstract":"<div><div>Maternal deprivation (MD) is a potent stressor during early life and can lead to behavioral changes during adulthood. Several neurochemical mechanisms underlying MD-induced stress have been proposed; among them is the damage caused to dopaminergic neurons in the ventral tegmental area (VTA). We hypothesized that pharmacological stimulation of dopaminergic neurons in VTA by the infusion of an N-Methyl-D-Aspartate (NMDA) receptors agonist (used considering the wide distribution of these glutamatergic receptors in the VTA neurons) can reverse MD-induced memory deficits. Here, we demonstrated that MD affects male and female rats distinctly, with females being more resilient to early-life stress. Furthermore, NMDA pharmacological stimulation of the VTA promotes object recognition (OR) memory persistence in male and female non-MD rats. In males, infusion of NMDA into the VTA immediately after the learning session reverses recognition memory deficits related to MD. Although MD female rats have not shown deficits in OR memory consolidation, the NMDA infusion immediately after the learning session promotes memory persistence. We verified that MD leads to memory deficits in adult male rats, while the females are resilient to early life stress. Furthermore, NMDA pharmacological stimulation of dopaminergic VTA neurons reveals the dopaminergic modulation of OR memory in MD rats, even in females that did not exhibit memory deficits.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1848 ","pages":"Article 149316"},"PeriodicalIF":2.7,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Depression unveiled: Insights into etiology and animal models for behavioral assessment, exploring the multifactorial nature and treatment of depression","authors":"Sachin More ,&nbsp;Mohammed Kaleem ,&nbsp;Rohini Kharwade ,&nbsp;Ali F. Almutairy ,&nbsp;Naiyer Shahzad ,&nbsp;Md Ali Mujtaba ,&nbsp;Murtada Taha ,&nbsp;Ajay Pise ,&nbsp;Ameeduzzafar Zafar ,&nbsp;Danish Mahmood","doi":"10.1016/j.brainres.2024.149313","DOIUrl":"10.1016/j.brainres.2024.149313","url":null,"abstract":"<div><div>Over the past century, significant shifts in daily living have led to an increased prevalence of mental disorders, often linked to hormonal imbalances. Among these, anxiety and depression stand out as prevalent diagnoses, particularly in industrialized nations. Depression, according to the DSM-5, is a heterogeneous condition that affects emotional, cognitive, and physical functioning, with symptoms including insomnia, sexual dysfunction, and weight changes. Cognitive theories of depression highlight its impact on judgment, decision-making, thinking, and focus. Depression’s multifaceted nature means that no two patients experience identical symptoms, risk factors, or treatment responses. The COVID-19 pandemic has exacerbated mental health issues, with social isolation, restricted contact, and altered daily routines contributing to increased anxiety and depression, especially among adolescents and young adults. The pandemic’s psychological toll underscores the need for effective treatment strategies for mental disorders. The physical manifestations of major depressive disorder (MDD) are associated with a heightened risk of developing various medical conditions, including metabolic disorders, cardiovascular disease, stroke, epilepsy, and dementia. This review provides a comprehensive exploration of depression and anxiety, covering their different types, epidemiology, potential causes, diagnostic criteria, and available treatment options. It delves into the role of pharmacological interventions and examines recent advancements to enhance therapeutic outcomes. Additionally, the review assesses the therapeutic potential of drugs, offering insights into their efficacy in treating these complex mental health disorders. By targeting the multifactorial etiology of depression through drug repurposing and new drug development, researchers aim to enhance treatment efficacy and achieve better outcomes for patients with depression.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1847 ","pages":"Article 149313"},"PeriodicalIF":2.7,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614693","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Acorus tatarinowii alleviates D-galactose-induced Alzheimer’s-like disease cognitive impairment and Aβ-induced pericytes dysfunction in mice","authors":"Tong Zhang ,&nbsp;Juan Yang ,&nbsp;Haiying Xu ,&nbsp;Yushuang Cao ,&nbsp;Xinyuan Du ,&nbsp;Lichen Guo ,&nbsp;Bing Liang ,&nbsp;Linlin Su ,&nbsp;Lijuan Chai ,&nbsp;Qing Yuan ,&nbsp;Limin Hu","doi":"10.1016/j.brainres.2024.149312","DOIUrl":"10.1016/j.brainres.2024.149312","url":null,"abstract":"<div><div>Pericytes regulate cerebral blood flow (CBF) and excess amyloid in the brain. Pericyte dysfunction may contribute to the pathology of Alzheimer’s disease (AD)<em>. Acorus tatarinowii</em> (AT), a Chinese medicine commonly used to treat AD, protects the central nervous system. However, whether AT can regulate pericyte function and ameliorate cognitive dysfunction remains unclear. We employed a novel target recognition assay, quantitative measurement of CBF, hematoxylin and eosin staining, immunofluorescence staining, and Western blot to investigate the role of AT in improving cognitive function in patients with AD. Additionally, we investigated the therapeutic potential of β-Asarone, the primary active compound in AT, for treating AD by modulating pericyte function using transmission electron microscopy, silver staining, electrical impedance, and other methodologies. The results revealed that administration of AT effectively alleviated the cognitive impairments induced by D-galactose in mice, as evidenced by enhanced CBF, improved histological characteristics of damaged brain tissue cells, increased expression of platelet-derived growth factor-β (PDGF-β), decreased Aβ accumulation via enhanced lipoprotein receptor-related protein 1 (LRP1), and reduced beta-site APP-cleaving enzyme 1 (BACE1). β-Asarone treatment mitigated ROS release and BACE1 expression while elevating the cell index in Aβ1-40 injured mouse brain vascular pericytes (MBVP). These findings suggest that AT has the potential to enhance CBF and mitigate pericellular dysfunction, thereby ameliorating Aβ deposition in the brain and improving cognitive impairment in patients with AD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1847 ","pages":"Article 149312"},"PeriodicalIF":2.7,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614668","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Naringin supplementation during pregnancy alters rat offspring’s brain redox system and mitochondrial function","authors":"B.G. dos Santos ,&nbsp;C.P. Klein ,&nbsp;P.M. August ,&nbsp;M.S. Crestani ,&nbsp;R.M. Hozer ,&nbsp;A.B. Saccomori ,&nbsp;B.M. Dal Magro ,&nbsp;K.S. Rodrigues ,&nbsp;C. Matté","doi":"10.1016/j.brainres.2024.149317","DOIUrl":"10.1016/j.brainres.2024.149317","url":null,"abstract":"<div><div>Naringin supplementation is known to ameliorate oxidative stress in the central nervous system (CNS) and improve cognitive function in disease models using adult rodents. However, if this supplementation is applied during critical periods of development, would it still be beneficial? To address this question, we used pregnant Wistar rats that were supplemented daily with naringin (100 mg/kg) during gestation. After delivery, pups were euthanized on postnatal day (PND) 1, 7, and 21. The prefrontal cortex, hippocampus, striatum, and cerebellum were dissected for redox system and mitochondrial function evaluation. Our data demonstrated that naringin supplementation to pregnant rats during gestation differentially affected the brain structures analyzed, inducing a dysregulation in the redox homeostasis, mainly on PND1. Redox and mitochondrial alterations found in offspring’s cerebellum on PND1 were also observed on PND7, and persisted up to PND21, indicating a higher susceptibility of this structure to the effects triggered by maternal naringin supplementation. In contrast to what was observed in the cerebellum, we found a progressive decline in the number of alterations in the prefrontal cortex, hippocampus, and striatum from PND1 up to PND21, suggesting that these brain structures are not as susceptible as the cerebellum to the naringin’s effects. Thus, our findings demonstrate a possible negative programming effect triggered by maternal naringin supplementation during pregnancy in the offspring’s brain, especially in the cerebellum.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1847 ","pages":"Article 149317"},"PeriodicalIF":2.7,"publicationDate":"2024-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142614675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Factors influencing language performance in boys and girls at age 2 in the French ELFE birth cohort","authors":"Frédérique Gayraud ,&nbsp;Jean-Louis Lanoë ,&nbsp;Maria De Agostini","doi":"10.1016/j.brainres.2024.149305","DOIUrl":"10.1016/j.brainres.2024.149305","url":null,"abstract":"<div><div>Different environmental and biological variables affect the rhythm of language acquisition in children. A substantial amount of literature has shown that girls overtake boys, at least in the early stages of language acquisition. The goal of this study is to investigate how different factors affect language scores in girls and boys. The parents of 6415 two-year-old French children from the ELFE cohort completed a parental questionnaire assessing language development. Our results show that girls do indeed display higher scores. In order to explore the impact of different variables – such as child characteristics, parental characteristics, the extent to which parents have interactions, such as reading and singing with children – on girls’ and boys’ scores, we tested logistic regressions contrasting children with very low scores with those with average or high scores. We found that sex remained a highly significant explanatory variable. Finally, we analyzed the extent to which there are differences between girls and boys in terms of the variables associated with a low score. Strictly exposed to the same unfavorable factors, girls with very low scores at two years master more words than boys with very low scores. Although different variables are significantly associated with a low score, sex remains a highly significant explanatory variable. Hence, our work contributes significantly to the debated issue of sex/gender influence on language acquisition.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1847 ","pages":"Article 149305"},"PeriodicalIF":2.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603090","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repeated high-dose esketamine in early postnatal rats leads to behavioural deficits with long-term modifications in white matter microstructural integrity","authors":"Lijie Zhou ,&nbsp;Xianlei Wang ,&nbsp;Tianyu Cao ,&nbsp;Yibo Li ,&nbsp;Sufang Jiang ,&nbsp;Lining Huang","doi":"10.1016/j.brainres.2024.149311","DOIUrl":"10.1016/j.brainres.2024.149311","url":null,"abstract":"<div><div>Esketamine is commonly used for sedation or general anaesthesia in infants and young children. However, repeated esketamine administration during periods of rapid brain growth and development may result in various pathophysiological and cognitive changes. Therefore, this study aimed to investigate the influence of recurrent esketamine exposure on long-term behavioural and white matter consequences. Seven-day-old (P7) male rats were allocated to control, high-, and low-dose groups. Behavioural paradigm assessment was conducted at P25–29. Diffusion tensor imaging revealed long-term effects on water diffusivity in the splenium and cingulum white matter of the corpus callosum at P30. Subsequent two-dimensional structure-tensor analysis of brain tissue sections stained with Luxol fast blue (LFB) showed marked changes in the white matter microstructure in rats after multiple exposures to varying esketamine doses. High-dose esketamine significantly reduced activity time and total distance in the open-field experiment. High-dose esketamine exposure might lead to impaired short-term memory in rats. Additionally, the high-dose group showed prolonged immobility time during the forced swimming test. On the balance beam, the high-dose group displayed more right turns and right-foot slips and lower time spent on the rotating bar, indicating motor defects, than did the other groups. Diffusion tensor imaging demonstrated a decreased water molecule diffusion ability in the corpus callosum in the high-dose group. LFB staining indicated microstructural differences in the white matter of animals in the high-dose group. These findings suggest that behavioural deficits in high-dose esketamine-treated rats are at least partially attributed to changes in the white matter microstructure.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1847 ","pages":"Article 149311"},"PeriodicalIF":2.7,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603101","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Electroacupuncture improves learning and memory deficits in diabetic encephalopathy rats by regulating the Nrf2/HO-1 pathway","authors":"Wei Wang ,&nbsp;Min Liu ,&nbsp;Huachun Miao ,&nbsp;Xin Gong ,&nbsp;Feng Han ,&nbsp;Liangbin Shi ,&nbsp;Xili Yan ,&nbsp;Zhiliang Xu","doi":"10.1016/j.brainres.2024.149309","DOIUrl":"10.1016/j.brainres.2024.149309","url":null,"abstract":"<div><h3>Background</h3><div>High blood sugar caused by diabetic encephalopathy(DE) can lead to excessive accumulation of reactive oxygen species in the brain, induce oxidative stress, and subsequently cause neuronal degeneration and apoptosis. The Nrf2/HO-1 signaling pathway is one of the most important pathways in oxidative stress response, but the precise mechanism of EA treatment for DE and its specific mechanism of action on the Nfr2/HO-1 pathway remain unclear.</div></div><div><h3>Methods</h3><div>Male Wistar rats were randomly assigned to four groups: normal, solvent, model, and EA, with 10 rats per group. A DE rat model was induced by intraperitoneal injection of streptozotocin. EA was applied to stimulate the “Zusanli” (ST36) and “Weiwanxiashu” (EXB3) points bilaterally, alternately for 30 min each, once a day for 4 weeks in the EA group. The rats’ fasting blood glucose(FBG) levels were measured with a glucometer. The Morris water maze was used to evaluate their learning and memory abilities. The morphology of neurons in the CA1 area of the hippocampus was observed by Nissl staining. Detection of protein expression of Nrf2 and HO-1 in the CA1 area of the hippocampus was performed by immunohistochemistry and immunoblotting.</div></div><div><h3>Results</h3><div>EA treatment reduced blood glucose levels, improved learning and memory abilities, increased the number of neurons in the hippocampal CA1 area, and upregulated the expression of Nrf2 and HO-1 in rats with DE. EA treatment may inhibit oxidative stress by modulating the Nrf2/HO-1 pathway in the hippocampal CA1 area, exerting a protective effect on neuronal cells in the hippocampal area in DE.</div></div><div><h3>Conclusion</h3><div>EA enhances the learning and memory abilities of rats with DE by regulating the Nrf2/HO-1 pathway in the CA1 area of the hippocampus. This indicates that EA has the potential to protect neurons by reducing oxidative stress.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1847 ","pages":"Article 149309"},"PeriodicalIF":2.7,"publicationDate":"2024-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}